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DONEPEZIL FOR DOWN'S

Sir,

A 56 years old woman suffering from Down's
Syndrome with moderate learning disability presented with increasing short
term memory problem, disorientation and episodes of agitation.

She was going to toilet but forgetting why she
went there and consequently she became incontinent of urine and faeces. She
was treated with antidepressant, which lifted her mood and resolved her
agitation.

However, her memory difficulties and progressive
loss in her complex living skills were causing concern to her carers. The day
centre she was attending was finding it difficult to manage her behaviour that
related to her memory disturbance. She has a family history of dementia and
her mother died of Alzheimer disease.

Since Donepezil has been found to be useful in
frontal lobe symptoms of dementia, it was thought that it might perhaps reduce
her challenging behaviour and slow the progress of the decline of her
dementia.

She was commenced on a small dose of Donepezil
i.e. 5mg Daily but unfortunately after 2 -1/2 weeks of it, she developed
behavioural problems, wandering at night, incontinence of urine and faeces and
got confused. She started lying on the floor hitting it with her fist. She
became agitated again.

Under the circumstances, the carers were not in
favour of continuing this medication as their perception was that it all
happened due to Donepezil although another carer did admit that she developed
similar behaviour when she was commenced on a small dose of Haloperidol.
However, respecting the wishes of her carers and their reluctance to
administer this medication anymore, it was stopped. Subsequently she improved
mood wise and became more manageable following the treatment of a Urinary
tract infection, which she happened to be suffering at that time.

We would like to know that did anybody anywhere
has any experience of using Donepezil to treat dementia in cases of learning
disability.

In spite of considerable achievement of
psychopharmacology and psychopharmacotherapeutics, there is opinion in the clinical
psychiatry, that psychopharmacotherapeutics is at the limit of its possibilities with the
current set of psychotropic medicines. We are interested in a pharmacology based on
specific combinations of caffeine, ironcontaining and nitric oxide producing.
As a result of our long term theoretical and experimental studies and clinical practice we
came up with a new original Concept of the complex psychopharmacotherapy of the variety
kind of mental disorders and a New Hypothesis on basic processes in the regulation of the
main intraneuronal metabolic processes and stipulation of possibilities for control of the
activity of such key intracellular regulatory enzymes as guanylate cyclase (GC) and
adenylate cyclase (AC).We hope to present the results of our recent theoretical,
experimental and clinical studies concerning this theme on the example of the treatment of
variety kind of depression as a future article in Psychiatry-on-line.

Clozapine and HIV+ Patients?

I am a Spanish psychiatrist working in a psychiatric
rehabilitation unit, which has 40 inpatients with an average stay between 6 and 12 months.
I have a schizophrenic patient, who is HIV+ . He has severe behavioural disorders with
aggressiveness. Treatment with conventional neuroleptics cause him important side effects
and Risperidone doesn't control his behavioural disorders. I am considering prescribing
Clozapine, but I am not sure if the haematological side effects of Clozapine may be
enhanced in HIV+ patients. Are there any readers who have experience in this issue?
I have done a bibliographical search in MEDLINE and I didn't find anything.
Yours sincerely

Has any reader any experience of treating treating
patients with DSM-IV diagnosis of Panic Attack and/or severe Social Phobia with Gabapentin
? The efficacy of Tricyclics, SSRI's, and MAOI's has been less than desirable in some
patients. Clonazepam has been strongly supplementing the anti-depressants, but significant
side effects, particularly severe short-term memory loss and sedation have made this less
than ideal for a number of patients. Gabapentin, however, as a GABA analog, would appear
to be an alternative, possibly offering efficacy similar to that of Clonazepam, without
sedation and memory effect.

Spectrum disorder seems to have become the acceptable, if not
fashionable, way of admitting our incompetence in distinguishing between mental illness
and 'normality'. Personality spectrum, schizophrenia spectrum, depressive spectrum,
whatever next? We appear to be moving further and further away from the fundemental idea
that there is a distinct break from normality to mental illness. This 'rainbow' approach
to diagnosis may well suit interior decoration but does nothing to further our patients
treatments. As an 'out-clause' for our not unusual treatment failures it may have some
merit, and also protect us from worry induced insomnia, but there is surely more utility
in definitive diagnosis, even if eventually modified. These tendencies seem to go hand-in
hand with our reluctance to diagnose personality disorder. "Depressed" we say
and 'treat' accordingly. So we empty our prisons and fill our ever shrinking hospitals.
Apart from the resulting eugenic disaster created by ill-conceived mixed wards, which have
become the norm despite any evidence of their benefit and much of their harm, what of the
financial implications? Is "diagnose or be damned" to be our new motto.

A meeting was held at St John of God Psychiatric hospital,
Sydney , Australia, recently and a hard copy of the e-mail I have received from the letter
published in Psychiatry On Line was handed to all concerned. This latter information
balanced the American position it was felt and there was general consensus to ;

1 not mandate Unilateral ECT as it was felt Bilateral ECT
is more effective and by using it there is often the need to have a larger number of ECT
and thus subject the patient to a greater risk in terms of a greater number of
anaesthetics.

2 Not mandate titration as it had been pointed out by
Dr Littlejohn, Consultant Psychiatrist in North Wales that sub threshold stimuli can cause
increased confusion and the process was thought to extend the anaesthetic for a longer
time while the titration took place.As he pointed out " why subject the patient to
this ? ".

3 Possibly reduce the dose on antidepressant medication but
make sure that other tranquillisers and other medication that could interfere with the ECT
process at a minimum. If one does not leave the patient on some antidepressant ( if the
patient is have the ECT for Major Depression ) there is the risk that the patient will
become depressed again in the time it takes to stabilise them after ECT is finished.

There were a number of other issues canvassed such as the
starting energy level for particular patients and generally it was felt that the age of
the patient is the best guide.I do not expect many psychiatrists will be using the stick
on electrode either in view of the pressure needed to hold them on during treatment.

The views obtained through the " Psychiatry on line
" have been a great help in this matter and they were able to be obtained quickly
which meant that they were able to be presented at the next ECT meeting and the special
committee that was formed to investigate all this has been disbanded now as all the issues
have been satisfactorily dealt with.

Dr Brian Boettcher

Consultant Psychiatrist

Original Letter

We are in the middle of reviewing ECT procedures in our
hospital ( St John of God Hospital , Burwood, Sydney Australia) Some of us recently went
to the Melbourne Clinic where they do 10-20 ECTs three times a week . They are into
titration of the dose (that is finding the threshold by slowly increasing the dose) and
unilateral ECT in high doses . What is the position in other countries on this ? Is
Unilateral in high dose better than low dose bilateral ? I gather the Royal College
recommended Bilateral in low dose some years ago but what is the current normal practice
in UK?I made some notes after the trip to Melbourne as follows :

Points

1. Unilateral high dose is the same as Bilateral in most
patients with the exception of the following who it may be should have bilateral from the
start;

Disturbed Manic patients

Patients who have had previous ECT and had to have Bilateral

Severely suicidally depressed

2. Unilateral should be the first choice in ECT ( with the
above exceptions) and only if there is a poor response should bilateral be

considered after a trial of Unilateral

3. Titration of the dose should start at 5 % under the age
of the patient and if no response should go up at 5% intervals until a response is
achieved ( the Melbourne Clinic starts at a lower level then this but it seems that it may
take too long to titrate )

4. Bilateral should start at half the unilateral dose and
titrated up also at 5% each attempt to have ECT.

5. Headaches are probably due to not enough relaxant .

6. One stimulus electrode can be lateral to the right eye (
if the person is left dominant ) and it is best if it is a stick on disposable electrode.

7. Skin for all electrodes , both stimulus and recording,
should be cleaned with the special solution " Pre Tac " or saline and then wiped
off.

8 Anti-depressants, and tranquilisers should be reduced or
ceased during ECT.

9. EEG bilateral recording is better than EEG and ECG
recording .

10 Imovane ( Zopiclone ) is better to use as a tranquiliser
during ECT as it does not interfere with the Epileptic fit as much. It does not have the
same respitatory depression nor affect the threshold for ECT as other tranquilisers.

We would be extremely interested in any comments readers
might make on this policy, compared to their national current opinion or local guidelines.

I read with interest Dr.Boza's comprehensive article on the
nature of hallucinations and illusions of non-psychiatric etiologies (1), but
found myself disagreeing with him on the concept of pseudohallucinations. Dr.Boza defined
the phenomena as "hallucinations that the patient knows as such; altough
perceptions are rather vivid and crisp, the patient has the insight that it has no
external foundation" (2). To my knowledge, the concept of
pseudohallucinations was coined by the German psychiatrist Karl Jaspers in the several
editions of his textbook "General Psychopathology" (3). To
Jaspers, pseudohallucinations were introspected images of great vividness. They were
considered figurative experiences, located in the inner eye (or ear) -the "internal
experiencial space", in sharp contrast with the perceptual disturbance found in true
hallucinations (4). Even though both phenomena could occur in the same patient
and be described as a single experience, Jaspers stressed the qualitative distinction
between them and accounted for the existance of a gradation between pseudohallucinations
and fantasy (imagery) experiences.

According to Sims (4), the confusion over the
meaning of these terms had arisen due to an a posteriori definition of
pseudohallucinations as self-recognized hallucinations (either "exterocepted" or
"introcepted"). However, this concept conflicts with the 1932 definition of the
French psychiatrist Henry Ey of hallucinosis, considered as "neurologic
hallucinations " in which a (true) perception without external object is criticized
by the patient (5).

Ethics Committees

My present problem is a crazy ethics committee which wants
reassurance that asking people about suicide will not "give them the idea".
Apart from the whole of psychiatric clinical experience, are there any relevant references
that I could use to deal with this lunacy.

It reminds me of the time the consumer representative
asserted that it was an invasion of the patient's privacy for us to look at the notes we
had written 5 years before. Any assistance would be most gratefully received. The measure
we are using is the Zung depression Scale to assess carers of patients with dementia. It
is the Zung which has caused angst for one member of the Management Board - i.e. because
carers will be asked about suicide. Despite the psychiatrist on the panel explaining that
the concern had not emerged as an issue in 30 years of clinical and research use of the
measure worldwide, I have been asked to travel from Sydney (where I live) to Adelaide (the
location of the host agency) to argue my case ... Otherwise, no study!

Stephen and Libby Judd libbyj@s054.aone.net.au

Native Americans

Sir,

As a Commanding Officer within the Navajo Indian Nation's Department
of Law Enforcement. I am searching for any and all materials, publications, etc. that
pertain to psychological disorders confronting Native Americans as the result of 130 years
of oppression and governmental dependancy. Thus far I have found nothing pertaining to
this subject matter. I would also be extremely interested in proposals to conduct research
related to a variety of aspects pertaining to Native American Social and Psychological
Disorders.

**A point to ponder is that this form of research has intentionally
been avoided.

Modecate and risperidone

The Psychiatric Hospital that I am involved with has a number of
psychiatrists who are using fluphenazine decanoate ( depot neuroleptic) and risperidone,
in middle range doses, together. We would be interested if readers feel could envisage any
situtations in which such a combination is reasonable?

Is there a risk of side effects that one could not respond to
quickly enough.

Auditing counselling in General Practice

I belong to a fund holding general practice that now provides quite
a range of psychological services: 2 counsellors, one specialising in substance abuse
(working on one to one basis but, also using groups), a CPN, a clinical psychologist, a
GP, trained in gestalt counselling (using one to one and groups) and a trainee counsellor.
We are proud of what we provide but would like to demonstrate that we are making a
significant effect and that we are worthwhile.

So some basic questions have emerged.

Does counselling in our practice do what it says we can do?

Who benefits and who does not?

Can effects be measured in a way that is repeatable, understood by
other professionals who may or may not be involved in counselling in primary care and who
may not be sympathetic towards counselling.

How long does any effect last? Are there ways of demonstrating change
beyond the immediate client? (ie family or job)

Lastly (for the moment!): could such a tool be useful to those
working at the cognitive end as well as those at the more psychodynamic pole?

Any resulting audit tool should be easy to use and acceptable to
patients and perhaps even be part of the therapy in its usefulness.

I am sure we are not alone in this quest and I would be interested
to hear of anyone who would like to help.

Yours sincerely,
Jeremy Vevers.

Dysfunctional Attitude Scale.

Sir,

Your On-line journal deeply impressed me and I hope that your many readers can help me. I
am a psychiatrist in South Korea. My main area of concern is cognitive therapy of
depression and now I am planning to study about depression symptoms and distorted
cognition of general population. I have been trying to locate article about Dysfunctional
Attitude Scale for 5 months and found many. But I can not locate paper about rating scale
itself and validity study. Now I know that author of this instrument is Dr. Weissman and
he presented many papers in many meetings but in Korea it is hard to assess papers
presented in scientific meetings. Does anybody have or know where I can get these articles
and where Dr. Weissman is . Also I want to get permission to translate this instrument
into Korean and use in my study. So I want to know how to get permission.

The articles are as follows:

Weisseman,A., & Beck, A.T.(1978, November). Development and
validation of the Dysfunctional Attitude Scale(DAS). paper presented at the 12th annual
meeting of the Association for the Advancement of Behavior Therapy, Chicago.
Weissman AN: The Dysfunctional Attitude Scale: A Validation Study, thesis. University of
Pennsylvania Graduate School of Arts and Science, Philadelphia, 1979.
Weissman, A.N. & Beck, A.T.(1978, March). Development and validation of the
Dysfunctional Attitude Scale; A preliminary investigation. Paper presented at the Annual
Meeting of the American Educational Research Association, Toronto, Canada.
Weissman, A.N. (1980). Assessing depressogenic attitudes: A validity study. Paper
presented at the 51st Annual Meeting of the Eastern Psychological Association, Hartford,
Connecticut.

Evidence-based psychiatry

Sir,

We recently attempted to replicate, on an acute psychiatric ward,
David Sackett's study (Ellis et al Lancet 346:407-410, 1995) of the proportion of primary
medical interventions based on randomised controlled trials or systematic overviews. We
found that there was evidence from randomised controlled trials or systematic overviews
for 65% of our primary interventions (which represented the most important attempt to cure
or alleviate the primary diagnosis). This compares favourably with the rate reported by
Ellis et al in general medicine (53%). However, I was struck by the relative poverty of
the evidence available for many of our interventions in psychiatry.

In 1971, Archie Cochrane declared that psychiatry was basically
inefficient: i.e. it uses large numbers of therapies for which there is limited evidence.
For example, in the UK, a psychiatrist can prescribe around 20 antipsychotic drugs
although, perhaps with the exception of clozapine, there is little evidence to tell them
apart. The clinician therefore selects his/her own favourite drug or uses some form of
brain chemistry theory or just plain trial and error. A similar situation exists for
antidepressants (consider the huge increase in SSRI prescribing despite the lack of clear
cut evidence of superiority). One of the main reasons for this is that new drugs are
introduced when they are shown to be superior to placebo but of equivalent efficacy to
established treatments (perhaps with fewer side effects). The comparative studies rarely
have sufficient power to clearly demonstrate even considerable differences in efficacy and
are highly prone to type 2 errors. For example, one of the main studies of acuphase
compared to haloperidol had only 20% power to detect a real difference of 20% (between 40%
and 60% improvement rates)

My suggestion is that there is a real need for some large,
pragmatic, simple randomised controlled trials in psychiatry to provide a firm evidence
base for our clinical decision making. These would need to be performed at least on a
national, and preferably an international, basis.

I would be interested in any comments on this from readers of
Psychiatry On-Line, and if there is any support for my proposal.